Necrosis Tamara Datsko associate Professor of Pathology, sectional course and forensic medicine

Autolysis Autolysis is disintegration of the cell by its own hydrolytic enzymes liberated from lysosomes. Autolysis can occur in the living body when it is surrounded by inflammatory reaction , or may occur as postmortem change in which there is complete absence of surrounding inflammatory response. Autolysis is rapid in some tissues rich in hydrolytic enzymes such as in the pancreas, and gastric mucosa; intermediate in tissues like the heart, liver and kidney; and slow in fibrous tissue.

Necrosis is defined as focal death along with degradation of tissue by hydrolytic enzymes liberated by cells. It is invariably accompanied by inflammatory reaction. Necrosis can be caused by various agents such as hypoxia, chemical and physical agents, microbial agents and immunological injury. Necrosis

Two essential changes bring about irreversible cell injury in necrosis – cell digestion by lytic enzymes and denaturation of proteins. These processes are morphologically identified by characteristic cytoplasmic and nuclear changes in necrotic cell. The cytoplasm appears homogenous and intensely eosinophilic. The nuclear changes include condensation of nuclear chromatin (pyknosis) whith may either undergo dissolution (karyolysis) or fragmentation into many granular clumps (karyorrhexis) Necrosis

Morphologically, 5 distinct types of necrosis are identified: COAGULATIVE NECRISIS. This is the most common type of necrosis caused by irreversible focal injury, mostly from sudden cessation of blood flow (ischaemia), and less often from bacterial and chemical agents. The organs commonly affected are the heart, kidney, and spleen. Types of necrosis

Grossly, foci of coagulative necrosis in the early stage are pale , firm , and slightly swollen. With progression , they become more yellowich, softer, and shruncen. Microscopically change results from 2 processes: denaturation of proteins and enzzymatic digestion of the cell/ But cell digestion liquefaction fail to occur. Eventually, the necrosed focus is infiltrated by inflammatory cells and the dead cells are phagocytosed leaving granular debris and fragments of cells.

LIQUEFACTION (COLLIQUATIVE) NECROSIS Liquefaction necrosis occurs commonly due to ischaemic injury and bacterial or fungal infections. It occurs due to degradation of tissue by the action of powerful hydrolytic enzymes. The common examples are infarct brain and abscess cavity. Grossly, the affected area is soft with liquefied centre containing necrotic debris. Later, a cyst wall is formed. LIQUEFACTION (COLLIQUATIVE) NECROSIS

LIQUEFACTION (COLLIQUATIVE) NECROSIS Microscopically, the cystic space contains necrotic cell debris and macrophages filled with phagocytosed material. The cyst wall is formed by proliferating capillaries, inflammatory cells, and gliosis ( proliferation glial cells) in the case of brain and proliferating fibroblasts in the case of abscess cavity. LIQUEFACTION (COLLIQUATIVE) NECROSIS

CASEOUS NECROSIS Caseous necrosis is found in the centre of foci of tuberculous infections. It combines features of both coagulative and liquefactive necrosis. Grossly, foci of caseous necrosis, as the name implies, resemble dry cheese and are soft, franular and yellowich. This appearance is partly attributed to the histotoxic effects of lopopolysacharides present in the capsule of the tubercle bacilli, Mycobacterium tuberculosis.

Classification of necrosises according to etiology Toxic Vascular Trophoneurotic Alergic Traumatic

Clinic-morphologic kinds of necrosis Coagulative (dry) Sekvestr Colikvative (hydropic, damp) Bedsore (пролежина) Gangrene Infarct

Microscopically, the necrosed foci are structureless, eosinophilic, and contain granular debris. The surrounding tissue shows characteristic granulomatous inflammatory reaction consisting of epithelioid cells with interspersed giant cells of Langhans or foreign body type and peripheral mantle of lymphocytes. CASEOUS NECROSIS

Fat necrosis is a special form of cell death occurring at two anatomically different locations but morphologically similar lesions. These are: following acute pancreatic necrosis, and traumatic fat necrosis commonly in breasts. FAT NECROSIS

Fat necrosis in either of the two intrances results in hydrolisis of neutral fat present in adipose cells into glycerol and free fatty acids. The damaged adipose cells assume cloudy appearance when only free fatty acids remain behind, after glycerol leaks out. The leaked out free fatty acids, on the outher hand, complex with calcium to form calcium soaps discussed later under dystrophic calcification. FAT NECROSIS

Fibrinoid necrosis or fibrinoid degeneration is characterised by deposition of fibrin-like material which has the stining properties of fibrin. It is encountered in various examples of immunologic tissueinjury, arterioles in hypertension, peptic ulcer etc. Microscopically, fibrinoid necrosis is identified by brightly eosinophilic, hyaline-like deposition in the vessel wall or on the luminal surface of a peptic ulcer. Local haemorrhages may occur due to rupture of these blood vessels. Fibrinoid necrosis

Fibrinoid necrosis

Gangrene is a form of necrosis of tissue with superadded putrefaction Gangrene is a form of necrosis of tissue with superadded putrefaction. The type of necrosis is usually coagulative due to ischaemia. On the other hand, gangrenous or necrotising inflammation is characterised by primarily inflammation provoked by virulent bacteria resulting in massive tissue necrosis. (gangrene lung, gangrenous appendicitis, and noma9cancrum oris). Gangrene

This form of gangrene begins in the distal part of a limb due to ischaemia. The typical example is the dry gangrene in the toes and feet of an old patient due to arteriosclerosis. Other causes of dry gangrene foot include thromboangiitis obliterans, trauma, ergot poisoning. It is usually initiated in one of the toes which is farthest from the blood supply, containing so little blood that even the invading bacteria find it hard to grow in the necrosed tissue. Dry gangrene

This occurs in naturally moist tissues and organs such as the mouth, bowel, lung, cervix, vulva etc. Diabetic foot is another example of wet gangrene due to high sugar content in the necrosed tissue which favours growth of bacteria. Bed sores occurring in a bed-ridden patient due to pressure on sites like the sarcum, buttocks and heels are the other important clinical conditions included in wet gangrene. Wet gangrene usually develops rapidly due to blockage of venous and less commonly arterial blood flow from thrombosis or embolism. Wet gangrene

The affected part is stuffed with blood which favours the rapid growth of putrefactive bacteria. The toxic products formed by bacteria are absorbed causing systemic manifestations of septicaemia, and finally death. The spreading wet gangrene lacks clear-cut line of demarcation and may spread to peritoneal cavity causing peritonitis. Wet gangrene

Gas gangrene is a special form of wet gangrene caused by gas-forming clostridia( gram-positive anaerobic bacteria) which gain entry into the tissues through open contaminated wounds, especially in the muscles, or as a complication of operation on colon which normally contains clostridia. Clostridia produce various toxins which produce necrosis and oedema locally and are also absorbed producting profound systemic manifestation. Gas gangrene

Gas gangrene

The end